title: Astragaloside IV protects heart from ischemia and reperfusion injury via energy regulation mechanisms.
abstract: OBJECTIVE
  This study was designed to investigate the protective potential of AS-IV against ischemia and I/R-induced myocardial damage, with focusing on possible involvement of energy metabolism modulation in its action and the time phase in which it takes effect.
  
  
  METHODS
  SD rats were subjected to 30 minutes LADCA occlusion, followed by reperfusion. MBF, myocardial infarct size, and cardiac function were evaluated. Myocardial structure and myocardial apoptosis were assessed by double immunofluorescence staining of F-actin and TUNEL. Content of ATP, ADP, and AMP in myocardium, cTnI level, expression of ATP5D, P-MLC2, and apoptosis-related molecules were determined.
  
  
  RESULTS
  Pretreatment with AS-IV suppressed MBF decrease, myocardial cell apoptosis, and myocardial infarction induced by I/R. Moreover, ischemia and I/R both caused cardiac malfunction, decrease in the ratio of ATP/ADP and ATP/AMP, accompanying with reduction of ATP 5D protein and mRNA, and increase in P-MLC2 and serum cTnI, all of which were significantly alleviated by pretreatment with AS-IV, even early in ischemia phase for the insults that were implicated in energy metabolism.
  
  
  CONCLUSIONS
  AS-IV prevents I/R-induced cardiac malfunction, maintains the integrity of myocardial structure through regulating energy metabolism. The beneficial effect of AS-IV on energy metabolism initiates during the phase of ischemia.
authors.affiliation: Tasly Microcirculation Research Center, Peking University Health Science Center, Beijing, China; Department of Integration of Traditional Chinese and Western Medicine, School of Basic Medical Sciences, Peking University, Beijing, China.
authors.forename: Lei
authors.initials: L
authors.lastname: Tu
authors.forename: Chun-Shui
authors.initials: CS
authors.lastname: Pan
authors.forename: Xiao-Hong
authors.initials: XH
authors.lastname: Wei
authors.forename: Li
authors.initials: L
authors.lastname: Yan
authors.forename: Yu-Ying
authors.initials: YY
authors.lastname: Liu
authors.forename: Jing-Yu
authors.initials: JY
authors.lastname: Fan
authors.forename: Hong-Na
authors.initials: HN
authors.lastname: Mu
authors.forename: Quan
authors.initials: Q
authors.lastname: Li
authors.forename: Lin
authors.initials: L
authors.lastname: Li
authors.forename: Yu
authors.initials: Y
authors.lastname: Zhang
authors.forename: Ke
authors.initials: K
authors.lastname: He
authors.forename: Xiao-Wei
authors.initials: XW
authors.lastname: Mao
authors.forename: Kai
authors.initials: K
authors.lastname: Sun
authors.forename: Chuan-She
authors.initials: CS
authors.lastname: Wang
authors.forename: Chang-Cheng
authors.initials: CC
authors.lastname: Yin
authors.forename: Jing-Yan
authors.initials: JY
authors.lastname: Han
mesh_terms: D000244:Adenosine Diphosphate / Q000378:metabolism; D000249:Adenosine Monophosphate / Q000378:metabolism; D000255:Adenosine Triphosphate / Q000378:metabolism; D000818:Animals; D017209:Apoptosis / Q000187:drug effects; D008297:Male; D015428:Myocardial Reperfusion Injury / Q000188:drug therapy / Q000378:metabolism / Q000473:pathology; D009206:Myocardium / Q000378:metabolism / Q000473:pathology; D006180:Proton-Translocating ATPases / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D012503:Saponins / Q000494:pharmacology*; D014315:Triterpenes / Q000494:pharmacology*; D019210:Troponin I / Q000096:biosynthesis
chemical_list: D012503:Saponins; D014315:Triterpenes; D019210:Troponin I; C052064:astragaloside A; D000249:Adenosine Monophosphate; D000244:Adenosine Diphosphate; D000255:Adenosine Triphosphate; D006180:Proton-Translocating ATPases
keywords: ATP 5D; cardiac function; energy metabolism; myocardial structure